Platelets are considered as significant players in innate and adaptive immune responses. The adhesion molecules they express, including P-selectin, CD40L, and CD42b, facilitate interactions with many cellular effectors. Upon interacting with a pathogen, platelets rapidly express and enhance their adhesion molecules, and secrete cytokines and chemokines. A similar phenomenon occurs after exposure of platelets to thrombin, an agonist extensively used for in vitro activation of these cells. It was recently reported that the dengue virus not only interacts with platelets but possibly infects them, which triggers an increased expression of adhesion molecule P-selectin as well as secretion of IL-1β. In the present study, surface molecules of platelets like CD40L, CD42b, CD62P, and MHC class I were evaluated at 4 h of interaction with dengue virus serotype 2 (DENV-2), finding that DENV-2 induced a sharp rise in the membrane expression of all these molecules. At 2 and 4 h of DENV-2 stimulation of platelets, a significantly greater secretion of soluble CD40L (sCD40L) was found (versus basal levels) as well as cytokines such as GM-CSF, IL-6, IL-8, IL-10, and TNF-α. Compared to basal, DENV-2 elicited more than two-fold increase in these cytokines. Compared to the thrombin-induced response, the level generated by DENV-2 was much higher for GM-CSF, IL-6, and TNF-α. All these events induced by DENV end up in conspicuous morphological changes observed in platelets by confocal microscopy and transmission electron microscopy, very different from those elicited by thrombin in a more physiological scenery.

Fractional electrodamage in A549 human lung cancer cells was analyzed by introducing a non-integer order parameter to model the influence of electrical stimulation on cellular behavior. Numerical simulations were conducted to evaluate the conversion of electrical energy to heat within A549 cancer cells, emphasizing the electrocapacitive effects and electrical conductivity in modulating dielectric properties. Using the Riemann–Liouville fractional calculus framework, experimental results were accurately fitted, demonstrating the non-integer nature of electrodamage processes. The study identified a strong dependency of electrical behavior on frequency, revealing a critical role of fractional dynamics in the dielectric breakdown and susceptibility of A549 cells to voltage changes. These findings advance our understanding of cellular responses to electrical fields and provide insights into applications in cancer diagnostics, monitoring, and potential therapeutic treatments.

Arboviruses (arthropod-borne viruses) are etiological viral agents mainly transmitted by arthropod vectors that pose a significant burden on the human public health systems worldwide, causing millions of infections every year; these viruses need to replicate in hematophagous arthropods, including numerous species of mosquitoes, ticks, and midges, among others. Important arboviruses for human and animal health include the dengue virus (DENV), Mayaro virus (MAYV), Rift Valley fever virus (RVFV), Zika virus (ZIKV), Yellow fever virus (YFV), chikungunya (CHIKV), and African swine fever virus (ASF), among other closely related viruses. These infectious agents can infect different hosts (invertebrate vectors and mammalian hosts), which requires avoiding two types of immune responses to continue and remain in nature. Arboviruses have sylvatic (vector to wild animals) and urban (vector to humans) transmission cycles and have developed mechanisms to overcome ecological and biological challenges, allowing them to take over the cellular machinery and successfully complete their replication cycle among hosts. Despite numerous pieces of evidence and studies, the mechanisms, molecules, and components involved in the arbovirus replication cycles are yet to be defined. This chapter will discuss viral replication processes, immune evasion, and vaccine development for arboviral families that are relevant to public health.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive human cancers and is characterized by a high frequency of activating KRAS mutations, most commonly KRASG12D. Yet oncogenic KRAS alone is insufficient for malignant progression, indicating that additional cellular and environmental factors shape disease evolution. Obesity is a major modifiable risk factor for PDAC and creates a chronic metabolic environment marked by excess nutrient and lipid availability, inflammation, and altered redox homeostasis. In acinar cells, these conditions can increase metabolic and mitochondrial stress, promoting reactive oxygen species (ROS) generation and molecular and organellar damage. Cellular responses to such damage, however, do not necessarily lead to either complete recovery or cell death. Antioxidant defenses, autophagy, mitochondrial quality control, proteostasis, and DNA repair can contain or process damage, allowing cells to remain viable despite persistent or incompletely resolved injury. Thus, cellular fitness under chronic stress may depend not only on the amount of damage generated, but also on the capacity to tolerate damage while maintaining sufficient function. Here, we conceptualize the relationship between damage burden and cellular fitness as a dynamic redox damage tolerance threshold. Transient metabolic and redox stress may allow acinar cells undergoing acinar-to-ductal metaplasia (ADM) to return toward homeostasis, whereas sustained metabolic stress, as occurs in obesity, in the presence of oncogenic KRAS may enable ADM cells to remain functional despite residual damage. Such persistence may increase the opportunity for additional alterations and progression toward pancreatic intraepithelial neoplasia (PanIN). This framework places cellular damage tolerance, rather than damage generation alone, at the center of early PDAC development and highlights the mechanisms that determine this threshold as potential therapeutic vulnerabilities.

This study examined the response of osteoblast-like cells to siloxane-based biohybrid materials obtained via the sol–gel process and modified with titania or with titania and calcium. The biohybrids’ ability to form apatite and their degradation process were assessed in vitro via immersion in PBS and SBF. Characterization was performed using XRD, FT-IR, and SEM. The Siloxane-Ti biohybrid exhibited rutile crystalline phase formation, high stability, and resistance to hydrolytic degradation, but did not induce apatite growth. In contrast, the Ca-containing biohybrid showed a vitreous structure with significant surface morphology changes and increased degradability. The Ca-modification enhanced the precipitation of apatite layers, which was attributed to the presence of Ti-OH and Si-OH groups. Immersion of the Siloxane-Ti-Ca biohybrids in PBS produced a flake-like apatite-like mineral structure from the first day of immersion, while immersion in SBF led to a cauliflower-like apatite structure after 28 days. Osteoblast response was evaluated through cell adhesion, proliferation, and differentiation on the hybrid materials. The Siloxane-Ti hybrid promoted osteoblast adhesion and proliferation, whereas the Siloxane-Ti-Ca reduced cell viability and osteonectin expression at 21 days. The Siloxane-Ti hybrid also increased osteonectin expression at early stages, with osteopontin and osteocalcin expression emerging at later stages, indicating progression from early to mature stages stimulated by the hybrid material. The findings suggest that titania enhances the biocompatibility of siloxane materials and shows significant potential for bone tissue regeneration without added growth factors.